Editor's Comment: The 2-day CPET studies conducted by Staci Stevens and Christopher Snell at the Workwell Foundation, and by Betsy Keller at Ithaca College, have shown deficits in oxygen uptake in ME/CFS patients. This study examined data from 440 participants and concluded that these deficits were indicative of reduced mitochondrial function. "The low oxygen extraction during exercise was also reported in mitochondrial pathology, systemic lupus erythematosus, HIV, and myophosphorylase deficiency." Significantly, the researchers did not find an association between exercise intolerance and deconditioning in ME/CFS patients.

BACKGROUND: The insufficient metabolic adaptation to exercise in Chronic Fatigue Syndrome (CFS) is still being debated and poorly understood.

METHODS: We analysed the cardiopulmonary exercise tests of CFS patients, idiopathic chronic fatigue (CFI) patients and healthy visitors. Continuous non-invasive measurement of the cardiac output by Nexfin(R) (BMEYE B.V. Amsterdam, the Netherlands) was added to the cardiopulmonary exercise tests. The peak oxygen extraction by muscle cells and the increase of cardiac output relative to the increase of oxygen uptake (DeltaQ'/DeltaV'O2) were measured, calculated from the cardiac output and the oxygen uptake during incremental exercise.

CONCLUSION: Low oxygen uptake by muscle cells causes exercise intolerance in a majority of CFS patients, indicating insufficient metabolic adaptation to incremental exercise. The high increase of the cardiac output relative to the increase of oxygen uptake argues against deconditioning as a cause for physical impairment in these patients.